J 2017

Different Densities of Na-Ca Exchange Current in T-Tubular and Surface Membranes and Their Impact on Cellular Activity in a Model of Rat Ventricular Cardiomyocyte

PÁSEK, Michal, Jiří ŠIMURDA and G. CHRISTÉ

Basic information

Original name

Different Densities of Na-Ca Exchange Current in T-Tubular and Surface Membranes and Their Impact on Cellular Activity in a Model of Rat Ventricular Cardiomyocyte

Authors

PÁSEK, Michal (203 Czech Republic, guarantor, belonging to the institution), Jiří ŠIMURDA (203 Czech Republic, belonging to the institution) and G. CHRISTÉ (250 France)

Edition

Biomed Research International, New York, Hindawi Publishing Corporation, 2017, 2314-6133

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

30400 3.4 Medical biotechnology

Country of publisher

United Kingdom of Great Britain and Northern Ireland

Confidentiality degree

není předmětem státního či obchodního tajemství

Impact factor

Impact factor: 2.583

RIV identification code

RIV/00216224:14110/17:00095655

Organization unit

Faculty of Medicine

UT WoS

000396222700001

Keywords in English

SODIUM-CALCIUM EXCHANGE; NA+-CA2+ EXCHANGE; CARDIAC MYOCYTES; FAILING HEARTS; NA/CA EXCHANGE; PROTEIN; CELLS; LOCALIZATION; MECHANISM; RELEASE

Tags

Tags

International impact, Reviewed
Změněno: 20/3/2018 18:31, Soňa Böhmová

Abstract

V originále

The ratio of densities of Na-Ca exchanger current (I-NaCa) in the t-tubular and surface membranes (I-NaCa-ratio) computed from the values of I-NaCa and membrane capacitances (C-m) measured in adult rat ventricular cardiomyocytes before and after detubulation ranges between 1.7 and 25 (potentially even 40). Variations of action potential waveform and of calcium turnover within this span of the I-NaCa-ratio were simulated employing previously developed model of rat ventricular cell incorporating separate description of ion transport systems in the t-tubular and surface membranes. The increase of I-NaCa-ratio from 1.7 to 25 caused a prolongation of APD (duration of action potential at 90% repolarisation) by 12, 9, and 6% and an increase of peak intracellular Ca2+ transient by 45, 19, and 6% at 0.1, 1, and 5Hz, respectively. The prolonged APD resulted from the increase of I-NaCa due to the exposure of a larger fraction of Na-Ca exchangers to higher Ca2+ transients under the t-tubular membrane. The accompanying rise of Ca2+ transient was a consequence of a higher Ca2+ load in sarcoplasmic reticulum induced by the increased Ca2+ cycling between the surface and t-tubular membranes. However, the reason for large differences in the I-NaCa-ratio assessed from measurements in adult rat cardiomyocytes remains to be explained.

Links

NV16-30571A, research and development project
Name: Klinický význam a elektrofyziologické zhodnocení mutace c.926C>T genu KCNQ1 (p.T309I) jako možné „founder mutation“ syndromu dlouhého intervalu QT